将胎儿去甲肾上腺素能移植到胺缺乏的基底前脑核中可恢复对血管紧张素的饮水反应。

Fetal noradrenergic transplants into amine-depleted basal forebrain nuclei restore drinking to angiotensin.

作者信息

McRae-Degueurce A, Bellin S I, Landas S K, Johnson A K

出版信息

Brain Res. 1986 May 21;374(1):162-6. doi: 10.1016/0006-8993(86)90405-1.

Abstract

6-Hydroxydopamine-induced catecholamine denervations in the organum vasculosum of the lamina terminalis and the median preoptic nucleus attenuate drinking responses to systemic angiotensin II (ANG II) injections. Transplanting catecholamines in these nuclei using fetal noradrenergic (NE) cell suspension restores ANG II-elicited thirst. These results emphasize the functional importance of NE neuronal systems in nuclei of the anteroventral third ventricle (AV3V) in mediating ANG II-induced drinking behaviors.

摘要

6-羟基多巴胺诱导终板血管器和视前正中核中的儿茶酚胺去神经支配，减弱了对全身注射血管紧张素II（ANG II）的饮水反应。使用胎儿去甲肾上腺素能（NE）细胞悬液将儿茶酚胺移植到这些核中可恢复ANG II引发的口渴。这些结果强调了前腹侧第三脑室（AV3V）核中NE神经元系统在介导ANG II诱导的饮水行为中的功能重要性。